Helicobacter pylori and Associated Diseases

Helicobacter pylori, a spiral shaped pathogenic bacterium, was first isolated by Barry Warren and Robin Marshall about 20 years ago, earning them a Nobel Prize in Physiology or Medicine in 2005. More than 50% of the world population harbour Helicobacter pylori in their upper gastrointestinal tract and Helicobacter pylori infection is now accepted as the cause of the most common form of chronic gastritis. The prevalence of infection inversely correlates with socio-economic status. When not treated, the infection will persist in the stomach of most people for decades, but as much as 80% of infected individuals will never experience clinical symp­toms despite having chronic gastritis. Histology shows active chronic inflammation with infil­tration of the lamina propria by lymphocytes and plasma cells, and infiltration of the mucous neck region by neutrophils. Lymphoid follicles can develop, sometimes causing mucosal nodu­larity on endoscopy. Approximately 10-20% of those colonized by Helicobacter pylori ulti­mately develop gastric and duodenal ulcers. It is also widely accepted that the infection is the triggering factor for multifocal atrophic gastritis and intestinal metaplasia, i.e. the changes that increase the risk for the intestinal type of gastric cancer. Helicobacter pylori has been clas­sified as a type I (definite) carcinogen by the WHO. Furthermore, most of the gastric MALT lymphomas are associated with Helicobacter pylori infection. The diagnosis of Helicobacter pylori infection is based on methods requiring gastric mucosa obtained by endoscopy (histology, rapid urease test, culture, polymerase chain reaction (PCR)) or non-invasive methods (serology, urea breath test). Its therapy consists of a combination of proton-pump inhibitors and var­ious antibiotics. Because of antimicrobial resistance, there are attempts to develop a vaccine that would prevent infection with Helicobacter pylori.